نتایج جستجو برای: excitotoxic neuronal damage

تعداد نتایج: 339314  

Journal: :American journal of physiology. Regulatory, integrative and comparative physiology 2014
Samantha Dayawansa Stacey Ruch Ralph Norgren

Rats with bilateral excitotoxic lesions of the parabrachial nuclei (PBN) fail to acquire a conditioned taste aversion (CTA), yet they retain the ability to express a CTA learned prior to incurring the damage. Rats with bilateral electrolytic lesions of the lateral hypothalamus (LH) also have CTA learning deficits. The PBN have reciprocal neural connections with the LH. This suggests that these ...

Excitotoxicity results in a significant increase in Ca2+ influx; essentially from open N-Methyl-D-aspartate receptors (NMDARs) channels that cause a secondary rise in the intracellular Ca2+ concentration. It is correlated with neuronal death induced by Ca2+ overload. Dysfunction of NMDARs is associated with excitotoxic neuronal death in neurodegenerative disorders. In this study, the effects of...

Journal: :Neuroscience 2006
J Niquet D-W Seo S G Allen C G Wasterlain

When excitotoxic mechanisms are blocked, severe or prolonged hypoxia and hypoxia-ischemia can still kill neurons, by a mechanism which is poorly understood. We studied this "non-excitotoxic hypoxic death" in primary cultures of rat dentate gyrus neurons. Many neurons subjected to hypoxia in the presence of blockers of ionotropic glutamate receptors developed the electron microscopic features of...

Journal: :Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 2000
G W Kim J C Copin M Kawase S F Chen S Sato G T Gobbel P H Chan

Excitotoxicity is implicated in the pathogenesis of several neurologic diseases, such as chronic neurodegenerative diseases and stroke. Recently, it was reported that excitotoxicity has a relationship to apoptotic neuronal death, and that the mitochondrial toxin, 3-nitropropionic acid (3-NP), could induce apoptosis in the striatum. Although striatal lesions produced by 3-NP could develop throug...

Journal: :Brain research 2000
M W Craighead H Boutin K M Middlehurst S M Allan N Brooks I Kimber N J Rothwell

Several studies have demonstrated that antagonists of the corticotrophin releasing factor (CRF) receptor markedly inhibit experimentally induced excitotoxic, ischaemic and traumatic brain injury in the rat, and that CRF expression is elevated in response to experimentally induced stroke or traumatic brain injury. CRF is also induced by the pro-inflammatory cytokine interleukin 1 (IL-1), which p...

2015
Hsiu-Ling Tsai Sue-Joan Chang

Epilepsy is a major neurological disorder characterized by spontaneous seizures accompanied by neurophysiological changes. Repeated seizures can damage the brain as neuronal death occurs. A better understanding of the mechanisms of brain cell death could facilitate the discovery of novel treatments for neurological disorders such as epilepsy. In this study, a model of kainic acid- (KA-) induced...

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